The long term objectives of this laboratory are to identify nutritional factors which contribute to, or could reduce, the high incidence of colon cancer in western cultures. Hypothesis: in BALB/c mice the growth of colon tumor CT-26 when implanted into the colon, a nutrition responsive site (NR), is enhanced by increasing dietary essential fatty acids (EFA). These effects are mediated via the cyclooxygenase pathway in the synthesis of prostaglandin (PG's) of the 1 and 2 series. Inhibition of tumor growth in the colon and of pulmonary colonization is related to inhibition of arachidonic acid metabolism in the cyclooxygenase pathway by the constituents of dietary marine oils, eicosopentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are utilized for PG's of the 3 series. These events, if indeed nutrition related, are less likely to occur when CT-26 is implanted in the mid scapula area, a nutrition non responsive site (NNR). Using CT-26 tumors implanted in colon (NR), and in mild scapula (NNR), various isocaloric nutritional lipid intervention are planned, including varying EFA with and without varying marine oils. Corollary studies are conducted in tissue culture with CT-26 cells. Nutritional interventions will be evaluated on tumor latency time, tumor growth, pulmonary colonization, metastatic potential, and the demise of the host. Effects of EFA, EPA, and indomethacin on prostaglandin synthesis and lipid profiles of tumors and tissues is assessed. These studies should provide: 1) an understanding of the relationship of EFA's to tumor growth and metastasis, 2) insights on the relationship of EPA and DHA inhibition of colon tumors, 3) data on the feasibility of mixtures of marine oil with other dietary lipids as colon tumor inhibitors, 4) guidelines for nutritional interventions aimed at colon tumor prevention, and the management of patients with colon cancer following resection in conjunction with radiation or chemotherapy.